FoxO1-mediated autophagy is required for NK cell development and innate immunity

Shuo Wang, Pengyan Xia, Guanling Huang, Pingping Zhu, Jing Liu, Buqing Ye, Ying Du and Zusen Fan ()
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Shuo Wang: CAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
Pengyan Xia: CAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
Guanling Huang: CAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
Pingping Zhu: CAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
Jing Liu: CAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
Buqing Ye: CAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
Ying Du: CAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
Zusen Fan: CAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences

Nature Communications, 2016, vol. 7, issue 1, 1-15

Abstract: Abstract Natural killer (NK) cells exert a crucial role in early immune responses as a major innate effector component. However, the underlying mechanisms of NK cell development remain largely elusive. Here we show that robust autophagy appears in the stage of immature NK cells (iNKs), which is required for NK cell development. Autophagy defects result in damaged mitochondria and accumulation of reactive oxygen species (ROS) that leads to apoptosis of NK cells. Autophagy protects NK cell viability during development through removal of damaged mitochondria and intracellular ROS. Phosphorylated Forkhead box O (FoxO)1 is located to the cytoplasm of iNKs and interacts with Atg7, leading to induction of autophagy. FoxO1 deficiency or an inactive FoxO1AAA mutant abrogates autophagy initiation in iNKs and impairs NK cell development and viral clearance. Therefore we conclude that FoxO1-mediated autophagy is required for NK cell development and NK cell-induced innate immunity.

Date: 2016
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DOI: 10.1038/ncomms11023

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